Special Report

Nutrition in Clinical Practice

Volume 0 Number 0
The Use of Visceral Proteins as Nutrition Markers: An October 2020 1–7
© 2020 American Society for
ASPEN Position Paper Parenteral and Enteral Nutrition
DOI: 10.1002/ncp.10588
wileyonlinelibrary.com

David C. Evans, MD, FACS, PNS1 ; Mark R. Corkins, MD, CNSC, FASPEN, AGAF,
FAAP2 ; Ainsley Malone, MS, RD, LD, CNSC, FAND, FASPEN3,4 ;
Sarah Miller, PharmD, BCNSP5 ; Kris M. Mogensen, MS, RD-AP, LDN, CNSC6 ;
Peggi Guenter, PhD, RN, FAAN, FASPEN7 ; Gordon L. Jensen, MD, PhD8 ;
and the ASPEN Malnutrition Committee1

Serum albumin and prealbumin, well-known visceral proteins, have traditionally been considered useful biochemical laboratory
values in a nutrition assessment. However, recent literature disputes this contention. The aim of this document is to clarify that
these proteins characterize inflammation rather than describe nutrition status or protein-energy malnutrition. Both critical illness
and chronic illness are characterized by inflammation and, as such, hepatic reprioritization of protein synthesis occurs, resulting
in lower serum concentrations of albumin and prealbumin. In addition, the redistribution of serum proteins occurs because
of an increase in capillary permeability. There is an association between inflammation and malnutrition, however, not between
malnutrition and visceral-protein levels. These proteins correlate well with patients’ risk for adverse outcomes rather than with
protein-energy malnutrition. Therefore, serum albumin and prealbumin should not serve as proxy measures of total body protein
or total muscle mass and should not be used as nutrition markers. This paper has been approved by the American Society for
Parenteral and Enteral Nutrition Board of Directors. (Nutr Clin Pract. 2020;0:1–7)

Keywords
adverse outcomes; albumin; critical care; inflammation; nutrition assessment; prealbumin; risk; visceral proteins

Introduction
Serum albumin and prealbumin (historically known as
transthyretin) have traditionally been used as nutrition lab-
oratory values (markers) to quantify the amount of plasma-
circulating proteins and, thereby, thought to reflect nutrition
status. The aim of this document is to correct the misconcep-
tion that these proteins reflect nutrition status; rather, they
are associated with inflammation and, thereby, are a compo-
nent of nutrition risk assessment. Nutrition risk assessment
may identify patients who do not yet demonstrate signs and
symptoms of malnutrition but are at risk for its subsequent
development if nutrition support is not provided in a timely
manner.1 For example, low visceral-protein levels may be
seen in a well-nourished individual admitted to an intensive
care unit (ICU) after traumatic injury. This patient is not
malnourished but is hypermetabolic and hypercatabolic
and will become malnourished if he/she does not receive
adequate early enteral and/or parenteral nutrition. Malnu-
trition (actual, diagnosed malnutrition) and nutrition risk

From the 1 System Nutrition Support Team, OhioHealth Trauma and Surgical Services, Columbus, Ohio, USA; the 2 Division of Pediatric
Gastroenterology, Le Bonheur Children’s Hospital, Department of Pediatrics, University of Tennessee Health Science Center, Memphis,
Tennessee, USA; the 3 Nutrition Services, Mount Carmel East Hospital, Columbus, Ohio, USA; the 4 American Society for Parenteral and Enteral
Nutrition, Silver Spring, Maryland, USA; the 5 Providence Saint Patrick Hospital, University of Montana Skaggs School of Pharmacy, Missoula,
Montana, USA; the 6 Department of Nutrition, Brigham and Women’s Hospital, Boston, Massachusetts, USA; the 7 Clinical Practice, Quality,
and Advocacy, American Society for Parenteral and Enteral Nutrition, Silver Spring, Maryland, USA; and the 8 Medicine and Nutrition, The
Larner College of Medicine, University of Vermont, University of Vermont Health Network, Burlington, Vermont, USA.
Financial disclosure: None declared.
Conflicts of interest: Kris M. Mogensen is a member of the ThriveRx Nutrition Advisory Board and the Baxter Indirect Calorimetry Advisory
Board and is a speaker for the Baxter iCAN Conference. David C. Evans is a speaker and consultant for Abbott, Alcresta, and Fresenius and a
consultant for Coram/CVS. Mark R. Corkins, Ainsley Malone, Sarah Miller, Peggi Guenter, and Gordon L. Jensen have no conflicts of interest to
disclose.
Received for publication May 29, 2020; accepted for publication September 15, 2020.
Corresponding Author:
Ainsley Malone, MS, RD, LD, CNSC, FAND, FASPEN, Nutrition Support Dietitian, Mount Carmel East Hospital, Columbus, OH, USA.
Email: ainsleym@nutritioncare.org
2 Nutrition in Clinical Practice 0(0)

Executive Summary

• Serum albumin and prealbumin are not components of currently accepted definitions of malnutrition.
• Serum albumin and prealbumin do not serve as valid proxy measures of total body protein or total muscle mass
and should not be used as nutrition markers.
• The serum concentrations of albumin and prealbumin decline in the presence of inflammation, regardless of
underlying nutrition status.
• Serum albumin and prealbumin declines must be recognized as inflammatory markers associated with “nutrition
risk” in the context of nutrition assessment rather than with malnutrition per se. Nutrition risk is broadly defined
as the risk of developing malnutrition and/or poor clinical outcomes if nutrition support is not provided.
• The role of serum albumin and prealbumin in monitoring delivery and efficacy of nutrition support remains
undefined. Their normalization may indicate the resolution of inflammation, the reduction of nutrition risk, a
transition to anabolism, or potentially lower calorie and protein requirements.

(at risk for malnutrition as previously described) include
either inadequate intake or risk of inadequate intake
of nutrients “caused by one or more of the following
factors: insufficient intake, impaired absorption, increased
nutrient requirements, and altered nutrient transport and/or
utilization.”2
Illness, infection, and inflammation have long been asso-
ciated with the loss of lean body mass, and recent studies
have confirmed significant loss of muscle size, cellularity,
and leg muscle protein in critical illness.3 Identifying the
presence and severity of inflammation is crucial to charac-
terizing and assessing malnutrition.2 Cytokines, produced
during inflammation, often result in anorexia, in large part
by impairing the ability to digest or absorb nutrients.4
Hospitalized patients with severe inflammatory responses
(defined as C-reactive protein [CRP] > 100 mg/L) did not
demonstrate a strong, measurable response to nutrition
support in a large randomized controlled trial.5 See Figure 1
below.
With the vast majority of nutrition screening and assess-
ment tools, characterization of disease burden or inflamma-
tion is considered a foundational criterion to appropriately
assess and diagnose malnutrition.6 Of the 3 etiologic types
of malnutrition proposed by The Academy of Nutrition
and Dietetics and the American Society for Parenteral
and Enteral Nutrition (ASPEN) consensus characteristics
for the identification of adult malnutrition,2 malnutrition
related to both acute and chronic disease is character-
ized by the presence of inflammation, whereas starvation-
related malnutrition is not.2 Inflammation is also recognized
as a key component in the definition of illness-related
pediatric malnutrition.7 Inflammation is often associated
with a negative nitrogen balance and an increased rest-
ing energy expenditure, resulting in increased protein and
energy requirements.4 This, coupled with illnesses leading
to poor appetite, anorexia, inanition, dysphagia, or other
clinical aspects, limit adequate nutrient intake and represent
significant nutrition risk faced by critically ill patients.
Any recommendations in this paper do not constitute
medical or other professional advice and should not be
taken as such. To the extent that the information published
herein may be used to assist in the care of patients, this is
the result of the sole professional judgment of the attending
healthcare professional whose judgment is the primary
component of quality medical care. The information pre-
sented here is not a substitute for the exercise of such
judgment by the healthcare professional. Circumstances in
clinical settings and patient indications may require actions
different from those recommended in this document, and in
those cases, the judgment of the treating professional should
prevail. This paper was approved by the ASPEN Board of
Directors.
Historical Use in Nutrition Assessment
Use of serum albumin in nutrition assessment was first
described by Blackburn et al in the classic 1977 publication,
“Nutritional and Metabolic Assessment of the Hospitalized
Patient,”8 as an important parameter in completing a nutri-
tion assessment. Serum proteins described for use with this
metabolic nutrition assessment included serum albumin and
serum transferrin or its derived marker, total iron-binding
capacity. The authors suggested that this nutrition assess-
ment process could be used to identify malnutrition, which
could influence morbidity and mortality. Subsequently,
serum albumin and transferrin became highly utilized mark-
ers to assess for malnutrition in hospitalized patients. In
1979, researchers recommended the use of serum albumin
as 1 of 2 biochemical parameters for an “instant nutrition
assessment” to identify those patients requiring aggressive
nutrition support.9,10 Serum albumin and/or transferrin
became standard components of nutrition assessment to
Evans et al
Figure 1. Relationship between malnutrition, inflammation, and visceral proteins.
diagnose malnutrition by those involved in clinical nutrition
support.11,12
Subsequently, serum transthyretin, or prealbumin,
emerged as a more sensitive nutrition marker because of
its shorter half-life of <2 days, as compared with albumin
(20 days) and transferrin (8 days). In 1996, Mears reported
finding that serum prealbumin was a more sensitive measure
of nutrition status compared with serum albumin.13
In the proceedings of a 1995 roundtable on measuring
protein status, serum prealbumin was emphasized to be the
preferred laboratory measurement to assess nutrition status,
as well as to monitor the response to nutrition therapy.14
At that time, advancements in clinical laboratories allowed
ready availability of serum prealbumin measurements,
which facilitated clinical nutrition use.
Relationship With Inflammation
Critical illness is characterized by severe acute
inflammation, whereas chronic illness is characterized
by a relatively lower but more prolonged, or intermittent,
inflammatory state. The acute-phase response may occur
in both acute and chronic illness and is evidenced by
changes in concentrations of various proteins mediated by
smaller molecules known as cytokines. Traditionally, the
affected proteins have been divided into 2 categories on
the basis of whether their serum concentrations increase or
decrease during the response. Those whose concentrations
increase are known as positive acute-phase proteins; these
include complement factors, various proteins involved in
coagulation and fibrinolysis, and CRP. Proteins whose
concentrations decrease include visceral proteins, such
3
as serum albumin, serum prealbumin (transthyretin), α 2 -
macroglobulin, and transferrin.15 Several early studies of
critically ill trauma and sepsis patients demonstrated rises
in positive acute-phase proteins and declines in negative
acute-phase proteins.16,17
The explanation posited for the decrease in visceral
proteins during the acute-phase response has generally been
that there is a hepatic reprioritization of protein synthesis,
resulting in redirected synthesis of the negative acute-phase
proteins toward synthesis of positive acute-phase reactants.
One of the most studied of the positive acute-phase pro-
teins, CRP, has been shown to have pleiotropic roles in both
proinflammation and anti-inflammation.15
This hepatic reprioritization of protein synthesis has
been theorized to be an indication that visceral proteins
may not be an essential component for host defense during
the acute-phase response, and their synthesis is a lesser
priority to the stressed host.18 However, this explanation
may be overly simplistic, as some evidence suggests that the
fractional albumin synthesis rate in the plasma (although
not necessarily in the whole body) may actually be increased
during the acute-phase response.19
Another important reason exists for the observed de-
crease in serum albumin plasma concentrations during the
acute-phase response. Albumin is the most abundant pro-
tein in human plasma. An increase in capillary permeability,
as it occurs in inflammatory states, leads to albumin leaving
the intravascular space (the compartment where concen-
trations are most commonly measured in clinical practice)
and entering the interstitial space.19,20 There may be func-
tional advantages to the redistribution of albumin during
the acute-phase response. Albumin is a key extracellular
4 Nutrition in Clinical Practice 0(0)
antioxidant.19 As such, it serves as a ligand for pro-oxidative
metals, such as copper and iron, as well as free fatty acids.
Increased amounts of albumin in the interstitium increase
the capacity of the protein to act as an antioxidant in this
space.
Yet another proposed mechanism for the decreased
concentration of visceral proteins, particularly serum al-
bumin, during the acute-phase response is increased tissue
catabolism.21 This accelerated breakdown may lead to a
decreased half-life of serum albumin.19 Other contributing
factors to declines in serum albumin concentrations could
include renal and gastrointestinal losses.19,21
Albumin is a major contributor to colloid oncotic pres-
sure. As hypoalbuminemia occurs in the intravascular space,
edema develops. Interstitial edema associated with low
serum albumin could lead to tissue damage, delayed wound
healing, impaired gastrointestinal function, impaired respi-
ratory gas exchange, impaired mobility, and resultant longer
hospitalization and a reduction in functional outcomes.22
In summary, serum concentrations of visceral proteins,
such as albumin and prealbumin, are decreased during the
acute-phase response associated with acute and chronic
illness and inflammation. Many of the clinical situations
in which nutrition support is utilized are characterized by
acute and/or chronic inflammation, and edema may be
present on examination.23 Clinicians must continue to rec-
ognize that decreased serum visceral-protein concentrations
do not reflect malnutrition but rather are the result of the
underlying inflammatory response.
Visceral Proteins as Markers of Nutrition
Status
Serum albumin and prealbumin continue to be incorrectly
cited as nutrition markers. Because of the strong associa-
tions between inflammation and malnutrition, visceral pro-
teins correlate well with patient risk for adverse outcomes
while not specifically reflecting a patient’s current nutrition
state.24 Inflammatory markers are useful for determining
nutrition risk by identifying those patients likely to be at
an increased risk of poor outcomes if adequate nutrition is
not delivered. For example, the Nutrition Risk in Critically
Ill tool for critically ill patients identifies those who have
an elevated risk of poor outcomes when adequate enteral
nutrition is not delivered.25 Malnutrition may be character-
ized by the type of inflammation present: acute illness/injury
or chronic illness. Relatively few patients in developed
countries have starvation-associated malnutrition, despite
the continuing presence of food insecurity and low-quality
diets deficient in protein.2
Serum albumin has historically been established as a
marker of surgical risk, and some surgical guidelines recom-
mend delaying surgery to allow time for nutrition support.26
A serum albumin level < 3.5 g/dL is associated with
increased postoperative mortality.27 A serum prealbumin
level < 10 mg/dL is associated with more complications after
free-flap surgery.28 Low serum prealbumin is also associated
with poor results after skin grafting.29 A large Veterans
Affairs database confirmed that a low serum albumin level
was associated with operative morbidity and mortality.30
Surgical-site infection, in particular, was associated with
hypoalbuminemia.30 Delay of surgery and initiation of
protein supplementation (or parenteral nutrition) was as-
sociated with improved biomarkers and improved clinical
outcomes.31 The European Society for Clinical Nutrition
and Metabolism recommends delay of surgery when the
serum albumin level is <3 g/dL.26 Although nutrition status
has historically been the focus, delaying surgery to allow the
resolution of inflammation with the use of sufficient nutri-
tion support may be the key factor. It has long been recog-
nized that patient outcomes are improved when any therapy
is delayed after an inflammatory event; a well-documented
example of this phenomenon is waiting to allow recovery
and resolution of inflammation before surgery to reverse a
colostomy after Hartmann procedure for diverticulitis.32,33
However, it must be recognized that sometimes surgery
is required to resolve an inflammatory process. This may
be true in conditions such as inflammatory bowel disease
or chronic infection of prosthetic implants, for example.
These patients should receive nutrition support and specific
treatments directed at inflammation and infection, when
possible, prior to surgery. Should they not improve and
require surgery in the setting of active inflammation, their
elevated risk of complications must be recognized and
mitigated, as possible.
Another common misconception is that serum albumin
and prealbumin are markers of protein and muscle mass in
body composition. Serum albumin and prealbumin levels in
healthy patients do not decline until their body mass index
(BMI) is <12 (calculated as weight in kilograms divided by
height in meters squared) after ≥6 weeks of starvation.34
The same is reported in elderly patients.35 Serum albumin
and prealbumin levels are known to correlate poorly with
nutrition intake—changes in dietary intake correlate poorly
with visceral proteins.36,37
Serum albumin and prealbumin levels have also been ex-
amined in children—in whom growth and development are
additional factors—with similar overall findings. Although
the visceral proteins retain similar correlations with inflam-
mation as they do in adult patients, there is poor correlation
with muscle mass or overall malnutrition assessments. One
study evaluating the nutrition status of 45 children at the
initial diagnosis of cancer compared anthropometrics with
serum albumin/prealbumin levels.38 Based on anthropomet-
rics, 49% of the patients were malnourished, but there was
no relationship with either serum albumin or prealbumin.
Another study evaluated critically ill children admitted to
a pediatric ICU.39 Anthropometrics were utilized for the
Evans et al
Table 1. Potential Nutrition Screening and Assessment Tools.
Nutrition screening MUST
Nutrition assessment SGA
Body mass index X X
Weight changes X X
Disease severity X X
Gastrointestinal symptoms X
Physical examination X
Mobility
Functional capacity X
Cognitive function
Aged > 70 years
Serum albumin
Developed by the author. Data are from references.50–54
MNA, mini nutritional assessment; MST, malnutrition screening tool; MUST, malnutrition universal screening tool; NRS-2002, nutrition risk
screening 2002; PON, perioperative nutrition screening tool; SGA, subjective global assessment.
diagnosis of malnutrition and were compared with serum
albumin levels. The study included 271 patients, with a 42%
malnutrition prevalence. Serum albumin level was signifi-
cantly associated with survival and duration of mechanical
ventilation. Multivariate analysis confirmed an association
of serum albumin with malnutrition. A more recent eval-
uation of children post–liver transplant found significantly
lower weight and height z-scores in those with confirmed
sarcopenia; however, the serum albumin levels were identical
regardless of alterations in body composition.40 Similar
findings were noted in preoperative evaluations of children
with Crohn’s disease. Children with severe malnutrition,
as defined by BMI-for-age z-scores, despite normal serum
albumin levels, had increased odds of complications, sim-
ilar to those with low serum albumin levels.41 A recent
evaluation of prealbumin in neonates in the neonatal ICU
demonstrated a negative correlation of −0.62 (P < .005)
with CRP, indicating the decrease in serum prealbumin was
associated with inflammation.42
Serum albumin and prealbumin have been evaluated as
nutrition markers in patients with restrictive eating disor-
ders, such as anorexia nervosa. A retrospective study eval-
uated 75 children with severe weight loss due to restrictive
eating disorders.43 These children were malnourished, with
a BMI z-score of −3.19. None of the patients had a low
serum albumin level and 32% had a low prealbumin level.
Despite the anthropometrics demonstrating malnutrition,
neither serum albumin or prealbumin level correlated with
BMI z-score.
Role of Visceral Proteins in Monitoring
Nutrition Support Efficacy
Research evaluating the utility of visceral proteins as
measures to assess efficacy of nutrition intervention has
5
NRS-2002 MST PON
MNA
X X
X X X X
X X X
X
X
X
X
provided mixed results. Early work in the 1980s by Ota44
and Winkler45 in cancer and surgical patients, respectively,
demonstrated serum prealbumin to be a more sensitive
indicator of adequate nutrition support compared with
other assessment parameters, including serum albumin and
transferrin. However, these results have not been confirmed
in subsequent studies and may have actually been a man-
ifestation of resolving inflammation. In 2012, Davis et al
evaluated the use of serum prealbumin in monitoring nu-
trition support efficacy in a large urban medical center.36 In
their analyses, serum prealbumin levels correlated only with
inflammation and did not reflect the delivery of adequate
energy and protein.36 Yeh et al demonstrated similar results
in patients receiving enteral nutrition.37 Despite the early
enthusiasm, serum prealbumin and other visceral proteins
have not been shown to be sensitive markers of energy and
protein intake adequacy and, therefore, should not be a
guide for therapeutic changes. The return of serum albumin
and prealbumin levels to normal ranges may still have value
in the monitoring of recovery. Normalization of visceral
proteins may indicate the resolution of inflammation, the
reduction of nutrition risk, a transition to anabolism, and
potentially lower calorie and protein requirements.
Alternatives for Nutrition Assessment and
Monitoring Efficacy
Numerous tools for nutrition assessment have been pro-
posed. A thorough discussion is beyond the scope of this
document, but there are various approaches that have been
suggested for outpatients, inpatients, and specific-disease
states. Most include a component of impaired oral intake
and/or weight loss (Table 1). Most of these tools do not
include visceral-protein parameters—the exception is the
perioperative nutrition screening tool (PONS) proposed by
6 Nutrition in Clinical Practice 0(0)
Wischmeyer et al, in 2018.46 The PONS tool is unique
because it is designed to evaluate preoperative outpatients
before surgery. The other measures in Table 1 are designed
for the inpatient setting and do not include serum albumin.
PONS has not been prospectively validated but relies on the
findings of Khuri et al that demonstrated serum albumin
levels are an excellent measure of surgical risk.27
Imaging represents a new frontier in nutrition as-
sessment. Dual-energy X-ray absorptiometry, bioelectrical
impedance, ultrasound, and computed tomography scan
are increasingly used for assessment of muscle mass. Each
tool has been validated in select populations but are lim-
ited either by availability, standardization, or validation in
relevant clinical populations.47 Imaging holds the potential
of emerging as a “biomarker” for standardized nutrition
assessment in the future as limitations are overcome.48 In
addition, the use of other assessment measures, including
creatinine height index, can be considered.49
Nutrition efficacy is an even more challenging param-
eter to measure. While in a state of acute inflammation,
adequate nutrition may mitigate weight loss, loss of muscle
function, and skin breakdown. Adequate nutrition may
be reflected by effective wound healing and resolution of
edema. Improvements in muscle strength and endurance
may be measured. However, meaningful gains in muscle
mass are unlikely in the acutely inflamed state; only after
inflammation subsides are such patients typically able to
achieve these gains.20
Conclusion
The visceral proteins albumin and prealbumin must be
correctly recognized as inflammatory markers associated
with “nutrition risk” in nutrition assessment. The concepts
of malnutrition and nutrition risk are distinct concepts
that are often inappropriately interchanged in application.
Serum albumin and prealbumin levels do not, however,
serve as proxy measures of total body protein or total
muscle mass and are not useful monitoring parameters
to guide nutrition support therapy. To identify these as
markers of malnutrition is an oversimplification that should
be avoided.
References
1. Zheng ZY, Heyland DK. Determination of nutrition risk and status
in critically ill patients: what are our considerations. Nutr Clin Pract.
2019;34(1):96-111.
2. White JV, Guenter P, Jensen GL, Malone A, Schofield M. Consensus
Statement: Academy of Nutrition and Dietetics and American Society
for Parenteral and Enteral Nutrition: characteristics recommended for
the identification and documentation of adult malnutrition (under-
nutrition). JPEN J Parent Ent Nutr. 2012;36(3):275-283.
3. Puthucheary ZA, Rawal J, McPhail M, et al. Acute skeletal muscle
wasting in critical illness. JAMA. 2013;310(15):1591-1600.
4. Sharma K, Mogensen KM, Robinson MK. Pathophysiology of critical
illness and role of nutrition. Nutr Clin Pract. 2019;34(1):12-22.
5. Merker M, Felder M, Gueissaz L, et al. Association of baseline inflam-
mation with effectiveness of nutritional support among patients with
disease-related malnutrition a secondary analysis of a randomized
clinical trial. JAMA Network Open. 2020;3(3):e200663. https://doi.org/
10.1001/jamanetworkopen.2020.0663.
6. Jensen GL, Cederholm TA, Correia MI, et al. The GLIM criteria
for the diagnosis of malnutrition – a consensus report from the
global clinical nutrition community. JPEN J Parenter Enteral Nutr.
2019;43(1):32-40.
7. Mehta NM, Corkins MR, Lyman B, et al. Defining pediatric malnu-
trition. JPEN J Parenter Enteral Nutr. 2013;37(4):460-481.
8. Blackburn GA, Bistrian BR, Maini BS, Schlamm HT, Smith MF.
Nutritional and metabolic assessment of the hospitalized patient.
JPEN J Parenter Ent Nutr. 1977;1(1):11-21.
9. Seltzer MH, Bastidas JA, Cooper DM, Engler P, Slocum B, Fletcher
HS. Instant nutritional assessment. JPEN J Parenter Enteral Nutr.
1979;3(3):157-159.
10. Seltzer MH, Fletcher HS, Slocum BA, Engler PE. Instant nutritional
assessment in the intensive care unit. JPEN J Parenter Enteral Nutr.
1981;5(1):70-72.
11. Hooley RA. Clinical nutritional assessment: a perspective. J Am Diet
Assoc. 1980;77(6):682-686.
12. Grant JP, Custer PB, Thurlow J. Current techniques of nutritional
assessment. Surg Clin North Am. 1981;61(3):437-463.
13. Mears E. Outcomes of continuous process improvement of a nutri-
tional care program incorporating serum prealbumin measurements.
Nutrition. 1996;12(7-8):479-484.
14. Bernstein L, Bachman TE, Meguid M. et al. Measurement of visceral
protein status in assessing protein and energy malnutrition: standard
of care. Nutrition. 1995;11(2):169-171.
15. Gabay C, Kushner I. Acute-phase proteins and other systemic re-
sponses to inflammation. New Engl J Med. 1999;340(6):448-454.
16. Peterson VM, Moore EE, Jones TN, et al. Total enteral nutrition
versus total parenteral nutrition after major torso injury: attenuation
of hepatic protein reprioritization. Surgery. 1988;104(2):199-207.
17. Clark MA, Hentzen BTH, Plank LD, Hill GH. Sequential changes in
insulin-like growth factor 1, plasma proteins, and total body protein
in severe sepsis and multiple injury. JPEN J Parenter Enteral Nutr.
1996;20(5):363-370.
18. JeVenn AK, Galang M, Hipskind P, Bury C. Malnutrition screening
and assessment. In Mueller CM ed. The ASPEN Adult Nutrition
Support Core Curriculum. 3rd ed. ASPEN; 2017:185-212.
19. Soeters PB, Wolfe RR, Shenkin A. Hypoalbuminemia: patho-
genesis and clinical significance. JPEN J Parenter Enteral Nutr.
2019;43(2):181-193.
20. Jensen GL, Bistrian B, Roubenoff R, Heimburger DC. Malnutrition
syndromes: a conundrum vs continuum. JPEN J Parenter Enteral
Nutr. 2009;33(6):710-716.
21. Kim S, McClave SA, Martindale RG, Miller KR, Hurt RT. Hypoal-
buminemia and clinical outcomes: what is the mechanism behind the
relationship? Am Surg. 2017;83(11):1220-1227.
22. Mendez CM, McClain CJ, Marsano LS. Albumin therapy in clinical
practice. Nutr Clin Pract. 2005;20(3):314-320.
23. Bernstein LH. The transthyretin inflammatory state conundrum. Curr
Nutr Food Sci. 2012;8(2):149-153.
24. Loftus TJ, Brown MP, Slish JH, Rosenthal MD. Serum levels of
prealbumin and albumin for preoperative risk stratification. Nutr Clin
Pract. 2019;34(3):340-348.
25. Rahman A, Hasan RM, Agarwala R, Martin C, Day AG, Heyland
DK. Identifying critically ill patients who will benefit most from
nutritional therapy: Further validation of the “modified NUTRIC”
nutritional risk assessment tool. Clin Nutr. 2016;35(1):158-162.
Evans et al
26. Weimann A, Braga M, Carli F, et al. ESPEN guideline: clinical
nutrition in surgery. Clin Nutr. 2017;36(3):623–650.
27. Khuri SF, Daley J, Henderson W, et al. Risk adjustment of the
postoperative mortality rate for the comparative assessment of the
quality of surgical care: results of the National Veterans Affairs
Surgical Risk Study. J Am Coll Surg. 1997;185(4):315-27.
28. Shum J, Markiewicz MR, Park E, et al. Low prealbumin level is a
risk factor for microvascular free flap failure. J Oral Maxillofac Surg.
2014;72(1):169-177.
29. Moghazy AM, Adly OA, Abbas AH, Moati TA, Ali OS, Mohamed
BA. Assessment of the relation between prealbumin serum level and
healing of skin-grafted burn wounds. Burns. 2010;36(4):495-500.
30. Gibbs J, Cull W, Henderson W, et al. Preoperative serum albumin level
as a predictor of operative mortality and morbidity: results from the
National VA Surgical Risk Study. Arch Surg. 1999;134(1):36–42.
31. Fleming FJ, Gillen P. Reversal of Hartmann’s procedure follow-
ing acute diverticulitis: is timing everything? Int J Colorectal Dis.
2009;24(10):1219-1225.
32. Keck JO, Collopy BT, Ryan PJ, et al. Reversal of Hartmann’s
procedure: Effect of timing and technique on ease and safety. Dis
Colon Rectum. 1994;37(3):243–248.
33. Hennessey DB, Burke JP, Ni-Dhonochu T, et al. Preoperative hy-
poalbuminemia is an independent risk factor for the development
of surgical site infection following gastrointestinal surgery: a multi-
institutional study. Ann Surg. 2010;252(2):325–329.
34. Lee JL, Oh ES, Lee RL. Finucane. TE Serum albumin and prealbumin
in calorically restricted, nondiseased individuals: a systematic review.
Am J Med. 2015;128(9):e1-1023.e22.
35. Bouillanne O, Phasaro H, Liabaud B, Duché C, Cynober L, Aussel C.
Evidence that albumin is not a suitable marker of body composition-
related nutritional status in elderly patients. Nutrition. 2011;27(2):165-
169.
36. Davis CJ, Sowa D, Keim KS, Kinnare K, Peterson S. The use of
prealbumin and C-reactive protein for monitoring nutrition support
in adult patients receiving enteral nutrition in an urban medical center.
JPEN J Parenter Enteral Nutr. 2012;36(2):197-204.
37. Yeh DD, Johnson E, Harrison T, et al. Serum levels of albumin and
prealbumin do not correlate with nutrient delivery in surgical intensive
care unit patients. Nutr Clin Pract. 2018;33(3):419-425.
38. Gurlek-Gokcebay D, Emir S, Bayhan T, Demir HA, Gunduz M,
Tunc B. Assessment of nutritional status in children with cancer and
effectiveness of oral nutritional supplements. Pediatric Hematol Oncol.
2015;32(6):423-432.
39. Leite HP, Rodrigues da Silva AV, de Oliveira Iglesias SB, Koch
Nogueira PC. Serum albumin is an independent predictor of clin-
ical outcomes in critically ill children. Pediatr Crit Care Med.
2016;17(2):e50-57.
40. Mager DR, Hager A, Ooi PH, Siminoski K, Gilmour SM, Yap
JYK. Persistence of sarcopenia after pediatric liver transplantation
is associated with poorer growth and recurrent hospital admissions.
JPEN J Parenter Enteral Nutr. 2019;43(2):271-280.
7
41. Ladd MR, Garcia AV, Leeds IL, et al. Malnutrition increases the risk
of 30-day complications after surgery in pediatric patients with Crohn
disease. J Pediatr Surg. 2018;53(11):2336-2345.
42. Tian T, Coons J, Chang H, Chwals WJ. Overfeeding-associated hy-
perglycemia and injury-response homeostasis in critically ill neonates.
J Pediatr Surg. 2018;53(9):1688-1691.
43. Huysentruyt K, De Schepper J, Vanbesien J, Vandenplas Y. Albu-
min and pre-albumin levels do not reflect the nutritional status of
female adolescents with restrictive eating disorders. Acta Paediatr.
2016;105(4):e167-169.
44. Ota DM, Frasier P, Guevara J, Foulkes M. Plasma protein as indices
of response to nutritional therapy in cancer patients. J Surg Oncol.
1985;29(3):160-165.
45. Winkler MF, Gerrior SA, Pomp A, Albina JE. Use of retinol-binding
protein and prealbumin as indicators of the response to nutrition
therapy. J Am Diet Assoc. 1989;89(5):684-687.
46. Wischmeyer PE, Carli F, Evans DC, et al. American society for
enhanced recovery and perioperative quality initiative joint con-
sensus statement on nutrition screening and therapy within a sur-
gical enhanced recovery pathway. Anesth and Anal. 2018;126(6):
1883–1895.
47. Mourtzakis M, Bell KE. Measures of sarcopenia: the utility of
ultrasound, bioelectrical impedance analysis and single-slice cross-
sectional imaging. In: Tandon P, Montano-Loza A, eds. Frailty and
Sarcopenia in Cirrhosis. Springer; 2020: 179-207.
48. Sheean P, Gonzales MC, Prado CM, McKeever L, Hall AM, Braun-
schweig CA. American Society for Parenteral and Enteral Nutrition
Clinical Guidelines: the validity of body composition assessment
in clinical populations. JPEN J Parenter Enteral Nutr. 2020;44(1):
12-43.
49. Bistrian BR, Mogensen KM, Christopher KB. Plea for reapplication
of some of the older nutrition assessment techniques. JPEN J Parenter
Enteral Nutr. 2020;44(3):391-394.
50. Ferguson M, Capra S, Bauer J, Banks M. Development of a valid and
reliable malnutrition screening tool for adult acute hospital patients.
Nutrition. 1999;15(6):458–464.
51. Guigoz Y. The mini nutritional assessment (mna®)review of the
literature – what does it tell us? J Nutr Health Aging. 2006;10(6):466-
485.
52. Jeejeebhoy KN, Keller H, Gramlich L, et. al. Nutritional assessment:
comparison of clinical assessment and objective variables for the
prediction of length of hospital stay and readmission. Am J Clin Nutr.
2015;101(5):956-965.
53. Kondrup J, Rasmussen HH, Hamberg O, Stanga Z; Ad HocE-
SPEN Working Group. Nutritional risk screening (NRS 2002): a new
method based on an analysis of controlled clinical trials. Clin Nutr.
2003;22(3):321-336.
54. Stratton RJ, Hackston A, Longmoe D, et al. Malnutrition in hospital
outpatients and inpatients: prevalence, concurrent validity and ease of
use in “the malnutrition screening tool” (MUST) for adults. Br J Nutr.
2004;92(5):799-808.